The synchronized holonomic model: A framework for efficient motion generation

We present a simple and efficient mathematical framework suitable for generating motion in the context of a variety of robotic motion tasks ranging from low-level motor control up to high-level locomotion planning. Our concept is based on a one-dimensional second-order model that allows analytic computation of its inverse dynamics while respecting physical constraints. This makes it a particularly useful tool for tasks that are expressed only as a start and goal state, such as animation key frames or way points in path planning. By means of time synchronization, the model extends easily to an arbitrary number of dimensions in a way that the target is reached in all dimensions at the same time. The framework excels in terms of execution time, which lies in the microsecond range even for high-dimensional trajectory generation tasks. We demonstrate our method in two different settings - full-body trajectory generation and path planning - and show its benefits in comparison with current state-of-the-art algorithms

Boundedness approach to gait planning for the flexible linear inverted pendulum model

In this paper, we take advantage of the Flexible LIP model that has shown to be more realistic w.r.t. the LIP for cost-eective or compliant biped robots for gait generation. We can use a stable inversion approach to obtain bounded Center of Mass (CoM) reference trajectories and show several advantages compared to preview control: avoidance of integration, lower computation time, exact tracking of reference Zero Moment Point (ZMP) trajectories and Capture Point determination

NER and HR pathways act sequentially to promote UV-C-induced germ cell apoptosis in Caenorhabditis elegans

Ultraviolet (UV) radiation-induced DNA damage evokes a complex network of molecular responses, which culminate in DNA repair, cell cycle arrest and apoptosis. Here, we provide an in-depth characterization of the molecular pathway that mediates UV-C-induced apoptosis of meiotic germ cells in the nematode Caenorhabditis elegans. We show that UV-C-induced DNA lesions are not directly pro-apoptotic. Rather, they must first be recognized and processed by the nucleotide excision repair (NER) pathway. Our data suggest that NER pathway activity transforms some of these lesions into other types of DNA damage, which in turn are recognized and acted upon by the homologous recombination (HR) pathway. HR pathway activity is in turn required for the recruitment of the C. elegans homolog of the yeast Rad9-Hus1-Rad1 (9-1-1) complex and activation of downstream checkpoint kinases. Blocking either the NER or HR pathway abrogates checkpoint pathway activation and UV-C-induced apoptosis. Our results show that, following UV-C, multiple DNA repair pathways can cooperate to signal to the apoptotic machinery to eliminate potentially hazardous cells